Exposure to fine particulate matter (PM2.5) has been associated with adverse cardiovascular outcomes. However, the effects of toxic metals in PM2.5 on cardiovascular health remain unknown. To investigate the early cardiovascular effects of specific PM2.5 metal constituents at the personal level, we conducted a panel study on 45 healthy college students in Caofeidian, China. Personal exposure concentrations and cardiovascular effect markers were monitored simultaneously within one year in four study periods. Four linear mixed-effects models were used to analyze the relationship between personal exposure to PM2.5 and 15 metal fractions (Al, V, Cr, Mn, Fe, Co, Ni, Cu, Zn, As, Se, Mo, Cd, Sb, and Pb) with soluble CD36 (sCD36), C-reactive protein (CRP), and oxidized low-density lipoprotein (OX-LDL) levels, heart rate, and blood pressure. The concentrations of most individual metals (Mn, Cu, Zn, As, Se, Mo, Cd, Sb and Pb) were the highest in winter. Meanwhile, there were significant differences in inflammatory (sCD36 and CRP) and oxidative stress (OX-LDL) markers in the serum of participants over the four seasons. In particular, the estimated effects of personal metal exposure (such as V, As, Se, Cd, and Pb) on sCD36 and pulse pressure (PP) levels were consistently significant across the four LME models. A significant mediating role of sCD36 was also found in the relationship between personal exposure to Zn and Cr and changes in PP levels. Our findings provide clues and potential mechanisms regarding the cardiovascular effects of specific toxic constituents of PM2.5 in healthy young adults.

Exposure to metals is associated with lung function decline. However, limited data are available about effects of co-exposure of metals on lung function. Additionally, the mechanism of the association between metals and lung function remains unclear. We conducted a longitudinal panel study in 2017–2018 among 45 healthy college students. Urinary 15 metals, lung function, biomarkers of oxidative stress and inflammation of participants were measured. Linear mixed effect (LME) and Bayesian kernel machine regression (BKMR) models were applied to explore the associations of urinary metals and mixture with lung function. Furthermore, we analyzed the mediating effect of biomarkers in the association between urinary metals and lung function. LME models showed the negative associations of aluminum (Al), vanadium (V), manganese (Mn), cobalt (Co), nickel (Ni), cadmium (Cd) or antimony (Sb) with Forced vital capacity (FVC), and V, Co, Ni, and Sb with Forced expiratory volume in one second (FEV1). BKMR models indicated the overall effect of metals mixture was negatively associated with FEV1 and FVC; urinary Sb was identified as the major contributor to decreased FVC and FEV1. Urinary 8-hydroxydeoxyguanosine mediated the association of Al, Mn, or Sb with FVC and the relationship of V with FEV1. The results revealed the longitudinal dose–response relationships of urinary metals with pulmonary function among healthy adults. Oxidative stress may be the underlying mechanisms of metals exposure associated with decreased lung function. Due to the small sample size, the interpretation of the results of this study should be cautious, and more studies are needed to verify the findings of this study.